STAT3 transcription factor, which is persistently activated in cancer cells and in diverse tumor-associated immune cells, is a critical mediator of tumorigenesis and immune evasion. As a convergence point for cytokine, growth factor and oncogenic kinase signaling, STAT3 is a highly desirable therapeutic target. However, pharmacological inhibition of proteins lacking enzymatic activity, such as STAT3, is challenging and requires alternative strategies. One of them is to block STAT3 DNA binding and transcriptional activation using competitive inhibitors, such as decoy oligodeoxynucleotides (dODN). Decoy ODNs comprise the specific, consensus sequence of the transcription factor binding site. The limiting factor in the clinical application of dODNs is difficulty in their targeted delivery, additionally complicated by the inherent sensitivity of the immune system to nucleic acids. However, immune cells may themselves be essential therapeutic targets in cancer therapy. We previously demonstrated that ligand for the intracellular receptor TLR9 (CpG ODN) allows for the delivery of oligonucleotides, such as siRNA, specifically to TLR9-positive target cells without any transfection or packaging reagents. Disclosed herein are solutions to these and other problems in the art.